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Is there evidence that low serotonin causes depression?




There is no convincing evidence that low serotonin levels are the main cause depression.. This is the conclusion of a “thorough” review by British researchers, overturning the widely believed belief that depression is the result of reduced levels or activity of chemicals. Researchers say the results cast doubt on the use of antidepressants.

“We have not found consistent evidence in the primary means of serotonin research that there is an association between serotonin and depression, and we also support the hypothesis that low serotonin activity or concentration is responsible for depression. “Not found,” said senior author Mark Horowitz, GDPsych, MBBS (Hons), PhD, Department of Psychiatry, University College, University of London, UK. Medscape Medical News..

“It is not an evidence-based statement that depression is due to a decrease in serotonin. If more honest and transparent to the patient, antidepressants may help paralyze the symptoms. I need to tell the patients, but it’s very unlikely that it will happen. It will be a solution or cure for their problem. “

Research Published online July 20 Molecular psychiatry.

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The theory that low serotonin levels may be the cause of depression was first proposed in the 1960s, but researchers note that it was only one of several hypotheses. Nonetheless, they report that it has become epidemic and “has been influential for decades and has provided an important justification for the use of antidepressants.”

The authors add that the introduction of selective reuptake inhibitors in the 1990s made the serotonin hypothesis widely publicized. According to a recent survey, over 80% of people believe in this theory.

“Most people think that depression is caused by a” chemical imbalance “or low serotonin in the brain. This is what many doctors say to people with depression, “Horowitz said.

“While it is known in academia that no good evidence of low serotonin in depression has been found so far, pharmaceutical marketing has amplified the’chemical imbalance’and the low serotonin hypothesis,” he said. I continued.

Question resolution

Horowitz et al. “Would you like to resolve this question by conducting a comprehensive, systematic and comprehensive review of all studies up to December 2020 on whether low serotonin levels are associated with depression?” rice field”. They investigated six hypotheses:

  • Low levels of serotonin and its metabolite 5-HIAA are found in the body fluids of people with depression.

  • Changes in serotonin receptor levels occur in people with depression.

  • High levels of SERT occur in people with depression.

  • Depression is triggered by the depletion of tryptophan, which reduces the available serotonin.

  • High levels of the SERT gene occur in people with depression.

  • In people with depression, there is an interaction between the SERT gene and stress.

Of the 361 publications, 17 were selected for inclusion in the review. These included meta-analyses, systematic reviews, genetically relevant studies, and comprehensive reviews of more than 165,000 patients.

To study the serotonin and 5-HIAA hypotheses, they looked at three large observation cohorts of postmenopausal women who investigated serotonin and 5-HT or 5-HIAA in plasma or cerebrospinal fluid (CSF). I turned to. Patients with depression had lower levels of plasma 5-HT, but after adjusting for multiple comparisons, the difference did not reach statistical significance.

A meta-analysis of 19 studies on 5-HIAA in CSF “found no evidence of an association between 5-HIAA levels and depression.”

5-HT1A Receptors block the release of serotonin before synapses. Therefore, when depression is caused by decreased serotonin activity due to receptor abnormalities, people with depression are expected to show “increased 5-HT activity.”1A Compared to those without receptors. “

However, the two meta-analyses showed no difference in 5-HT.1A If the levels of receptors between depressed persons or controls, or their inhibitory receptors, are low, “this means that depressed persons have high levels or activity of serotonin.”

Patients in these studies were taking or have recently taken antidepressants, which may have affected their findings.

The SERT protein transports serotonin from synapses, thereby reducing synaptic availability. Three overlapping meta-analyses suggested a potential reduction in SERT binding in some brain regions, but findings were inconsistent between reviews: “Effects of antidepressants and other medications. Cannot be excluded. “

“Various levels [5-HT1A] Receptors were the cause of depression, so low receptors reduce serotonin activity. However, neuroimaging of serotonin receptors in the brain showed no difference between people with and without depression, “Horowitz said.

“Suspect’s Statement”

Tryptophan depletion is thought to reduce serotonin and is being used to investigate whether lower levels of serotonin can lead to depression, Horowitz said.

However, a systematic review of meta-analysis and tryptophan depletion studies found that a small meta-analysis of people with a family history of depression was experienced by people who were actively depleted, but depletion participated. Significant depression in a person’s mood compared to those who have undergone fake treatment, which has shown no effect in inducing depression.

Another study found no difference between patients with a family history of depression and those without, and two crossover studies of depression and those who received current or recent antidepressant treatment “convinced” depletion. There is no powerful effect. “

A genetic theory has been proposed that suggests a “potential association” between depression and repetitive length polymorphisms in the promoter region of the SERT gene (5-HTTLPR), and recently gene polymorphisms “may cause only gene polymorphisms”. It was superseded by the suggestion that there is. Depression in the presence of stressful life events. “

Two large studies did not show an association between SERT gene polymorphisms and depression, or an interaction between the SERT gene and depression stress.

“Because depression is, of course, a complex emotional and behavioral state that contains chemicals, it is probably a very doubtful statement that chemicals” cause “depression, but they can be identified by a single chemical. The idea is very unlikely, “says Horowitz. ..

“A single chemical that causes depression because of the strong evidence that our living conditions, such as stressful life events, poverty, work anxiety, and relationships, have a strong impact on the risk of depression. This endless search of is probably looking for the wrong place.

“Our time is spent better by changing the circumstances that lead to depression than trying to decipher the chemical equations for depression.”

In one release, the study’s lead researcher, Professor Joanna Moncliffe, a psychiatrist at the University College of London’s University College of Psychiatry, said the findings cast doubt on the use of antidepressants.

“Currently, the majority of the UK population uses antidepressants. Thousands of people suffer from side effects such as severe withdrawal symptoms that can occur when people try to stop antidepressants. However, prescription rates continue to rise. This situation is being driven by the promotion of the false belief that depression is due to chemical imbalances. The public that this belief is not science-based. It’s time to let them know. “

Incomplete understanding

comment Medscape Medical NewsRoger McIntyre, a professor of psychiatry and pharmacology at the University of Toronto, Canada, and head of the Mood Disorder Psychopharmacology Unit, said that science is still “very much about the etiology of major depressive disorders.” Admitted that there is an “incomplete understanding”.

But “it’s also true that over the last 70 years, many have benefited from antidepressants known to target the serotonin system, which is probably due to serotonin dysregulation MDD.” .. McIntyre, chairman and executive director of the Brain and Cognitive Discovery Foundation in Toronto, who was not involved in the study, said.

“Despite the logic of that conclusion, there are clearly many assumptions inherent in it,” he continued. “Maybe the worn-out metaphor is Tylenol. headache, You probably won’t conclude that the headache is due to Tylenol deficiency. “

But he said he was concerned that without a deeper understanding of the underlying mechanisms of major depression, some could misunderstand the study and stop prescribing antidepressants. I added.

“The serotonin hypothesis of depression is not yet fully understood, [but that] It does not deny the efficacy, safety and tolerability of serotonin-based antidepressants. “

“We need better knowledge of the illness, and sometimes serotonergic regulation can help depression. We certainly need better treatment and are not constrained by the serotonin paradigm. You need to be careful, “concludes McIntyre.

This study is not specially funded. Horowitz is supported by a clinical research fellowship at the North East London NHS Foundation Trust. Other authors do not disclose the relevant financial relationships. McIntyre is supported by research grants from the CIHR / GACD / National Natural Science Foundation of China and the Milken Institute. Lundbeck, Janssen, Alkermes, Neumora Therapeutics, Boehringer Ingelheim, SageBiogen, Mitsubishi Tanabe Pharma, Purdue, Pfizer, Otsuka, Takeda, Neurocrine, Sunovion, Bausch Health, Axsome, Novo Nordisk, Kris, Sanofi, Eisai, Intra-Cellular, NewBridge Pharmaceuticals, Viatris, AbbVie, Atai Life Sciences CEO of Braxia Scientific Corporation

Mol psychiatry. Published online on July 20, 2022. Full text

Batya Swift Yasgur, MA, LSW are freelance writers counseling in Teaneck, NJ. She regularly contributes to many medical publications, including Medscape and WebMD, including consumer health books and Behind the Burqa: Our Livesin Afghanistan and How We Escaped to Freedom. Is also the author of. She was the sister who told her about them).




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